Research Articles

Research Articles

These pages on research articles are now reorganized into separate pages for each category. Doing this has been needed for some time, but it is with some trepidation we do this because in some diseases the research is very equivocal and incomplete.

While you may be on this site for MS, CFS or FMS, it is the pattern of ALL the research that provides the depth and impressive volume about CPn and how it causes chronic human disease that makes the picture clear. Don't make the mistake of thinking this is some new idea or that it has only a few studies just because it is relatively unknown in one field and the page on your specific disease includes only a couple of studies. This is as significant to human disease as understanding staphylococcus, only we are talking in this case about chlamydia pneumoniae.

Information about the germ applies and transfers from one field to the next: the important thing is to understand the pathogen and how it reacts in the body. Of interest you will find the material in the general, clamydia pneumoniae bacterial research, and the cardiac sections provide a very great depth. Read these sections in addition to the one related to your disease and you will be miles ahead. Of course I recommend reading all of this stuff it is interesting!

And hey we can add to this with so much room now so send along anything you think ought to go in....
Marie

General information : read this section for general information on chlamydia pneumoniae

Chronic Fatigue and Fibromyalgia

Multiple Sclerosis

Alzheimers and CPn

Cardiovascular Issues and Chlamydia pneumoniae Please do read THIS material even if you are here for something other than cardiovascular problems!

Arthritis and Chlamydia pneumoniae

Respiratory Issues and Chlamydia including asthma

CPn and other diseases Lots of interesting stuff here! interstitial cystitis, protstate enlargement....check it out

Lab analysis of Chlamydia Pneumoniae This is an important read for everyone

Antibiotic research in CPn This section contains links and abstracts of research on how antibiotcs affect CPn in different stages as well as research on how the antibiotics recommended for CAPs penetrate various tissues.

Porhyria and CAPs

Endotoxin Research Of interest to the person in treatment

Chlamydia Pneumoniae Bacterial Research Don't miss this section no matter what you are here for!

Supplements Research and monographs for Natural substances usd in the protocols

Vitamin D Vitamin d is now on its own page

Chlamydia Pneumoniae Miscellaneous related material

Polymicrobial Aspects /Research This section is for the curious and serious investigator and will be of less interest to those who just want to do the treatment. It has become clear that there are some important implications for the person infected with more than one pathogen and that this is common. The combination of one or more pathogens that live and "work" symbiotically may possibly be the key to how people can have something like MS.

mrhodes40 Wed, 2005-08-24 20:38

Comments

Alzheimers and Chlamydia Pneumoniae

Alzheimers and Chlamydia Pneumoniae

CPn infection promotes transmigration of monocytes through human brain endothelial cells

Chlamydophyla (chlamydia)pneumoniae in the AD brain More work by Brian Balin. Once again we see very good evidence of CPn being a neural pathogen.

Chlamydia pneumoniae in the alzheimers brain This work is on AD but the authors discovered CPn in the cells of the brain near the AD plaques. This should help establish CPn as a potentially neural pathogen

-Chlamydia pneumoniae in the Alzheimer's brain varies with APOE genotype The APOE genotype apparently interacts with CPn in alzheimers patients carrying that genotype. This suggests an interesting theory: that a bacteria is not the same in every person in terms of effects but rather an interaction between genes and bugs results in the pathology an individual experiences. This is a whole new understanding of how we interact with our environment.

The Balin research related to CPn in Alzheimer's Disease This list of research abstracts with links is an important study for anyone interested in CPn in the brain. Of note, this researcher like Dr Sriram also finds CPn in the brain consistently when others do not. This is likely due to the fact that both VU and Balin use frozen, not formalin fixed, tissue.

High prevalence of CPn antibodies in vascular dementia While VD is not alzheimers it is another indication that CPn has an affinity for cerebral tissue and is related to loss of brain integrity

mrhodes40 Sat, 2006-06-03 16:11

Chlamydophila pneumoniae cultured from the late-onset Alzheimer brain

Int J Med Microbiol. 2008 Sep 29. [Epub ahead of print]Click here to read

Initial characterization of Chlamydophila (Chlamydia) pneumoniae cultured from the late-onset Alzheimer brain.

Dreses-Werringloer U, Bhuiyan M, Zhao Y, Gérard HC, Whittum-Hudson JA, Hudson AP. Department of Immunology and Microbiology, Wayne State University School of Medicine, Gordon H. Scott Hall, 540 East Canfield Avenue, Detroit, MI 48201, USA.

Previous studies from this laboratory provided evidence that the intracellular bacterial pathogen Chlamydophila (Chlamydia) pneumoniae is present in the late-onset Alzheimer's disease (AD) brain. Here we report culture of the organism from two AD brain samples, each of which originated from a different geographic region of North America. Culturable organisms were detectable after one and two passages in HEp-2 cells for the two samples. Both isolates, designated Tor-1 and Phi-1, were demonstrated to be authentic C. pneumoniae using PCR assays targeting the C. pneumoniae-specific genes Cpn0695, Cpn1046, and tyrP. Assessment of inclusion morphology and quantitation of infectious yields in epithelial (HEp-2), astrocytic (U-87 MG), and microglial (CHME-5) cell lines demonstrated an active, rather than a persistent, growth phenotype for both isolates in all host cell types. Sequencing of the omp1 gene from each isolate, and directly from DNA prepared from several additional AD brain tissue samples PCR-positive for C. pneumoniae, revealed genetically diverse chlamydial populations. Both brain isolates carry several copies of the tyrP gene, a triple copy in Tor-1, and predominantly a triple copy in Phi-1 with a minor population component having a double copy. This observation indicated that the brain isolates are more closely related to respiratory than to vascular/atheroma strains of C. pneumoniae.

wow, yikes, good to know, something I have been speculating about.

 

Thanks for the post JimK

peace

 

CFIDS/ME, FMS, MCS, IBS, EBV, CMV, Cpn, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplements+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyl/day-5 days<

Cpn and Alzheimers

Here is an interesting article about the link between Cpn and Alzheimers: http://tinyurl.com/76bsby

I don't think it has been postted yet--if it has let me know.

Raven

Raven- Glad you found this. I'm going to link it to the Research book as it's a really clear, comprehensible report of Balin's work. Thanks.

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Jim, this is a deeply personal issue for me. Here I was on CAP treatment and I couldn't get my mom to consider treatment for my dad who had Alzheimers. Perhaps at that point it would not have made any difference but I sometimes feel I should have really pushed them on the issue. Nothing can be done now but I do miss him.

And I have not had any luck getting my mom to look at her infection. I even made an appointment for her with Dr. P. but she backed out at the last moment with the excuse he didn't take her type of insurance (which was an excuse as she could afford to pay up front). I have been able to get her to take the supplements but she is constantly battling respiratory infections,neurological pain and arthritis.

It has been important for me to accept what is/was and that I could not change it. But I have made a committment to being an activist for others and spreading the word when I can. My heart goes out to all those families who deal with this terrible condition. But from what we know now, there is probably an answer to the problem in the CAP treatment.

Wishing you a great New Year!

Raven

Feeling 98% well-going for 100. Very low test for Cpn. CAP since 8-05 for Cpn/Mycoplasma P.,Lyme, Bartonella, Mold exposure,NAC,BHRT, MethyB12 FIR Sauna. 1-18-11 begin new treatment plan with naturopath

Jim, I never heard back from Balin, but perhaps he's been lurking here. I'll keep sending him info periodically, regardless.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

thanks Raven, I sent this off to my husband, hopefully he reads it as he isn't treating as yet.

Good Job MacK, I hope Dr. Balin is lurking here & I am glad you are sending reminders.

 

peace

r

 

CFIDS/ME, FMS, MCS, IBS, EBV, CMV, Cpn, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplements+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyl/day-5 days<

Little by little this bacterium will reveal its nefarious activity.   Hopefully in time more research will be done about it and the diseases it causes.

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

Arthritis and Chlamydia Pneumoniae

Arthritis and Chlamydia Pneumoniae

Doxycycline versus doxycycline and rifampin in undifferentiated spondyloarthropathy, with special reference to chlamydia-induced arthritis a; 9 month studyA combinaiton protocol is effective here vs a monotherapy.

-Antibiotic treatment of arthritis Osteoarthritis when treated with doxycycline has significantly reduced joint space narrowing 40% better than controls.

Persisitant CPn and Arthritis Great paper overviews the concept of CPn and C. trachomatis as causitive agents in arthritis.

Sjogren's and CPn

mrhodes40 Sat, 2006-06-03 16:23

Chlamydia pneumoniae--a new causative agent of reactive arthritis and undifferentiated oligoarthritis

Chlamydia pneumoniae--a new causative agent of reactive arthritis and undifferentiated oligoarthritis

Find the article at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1005260

Abstract
OBJECTIVE--To examine whether reactive arthritis (ReA) known to occur after a urogenital infection with Chlamydia trachomatis can also follow an infection with Chlamydia pneumoniae, a recently described species of Chlamydiae that is a common cause of respiratory tract infections. METHODS--Specific antibodies (microimmunofluorescence test) and lymphocyte proliferation to C trachomatis and C pneumoniae in paired samples of peripheral blood and synovial fluid were investigated in 70 patients with either reactive arthritis (ReA) or undifferentiated oligoarthritis (UOA). RESULTS--Five patients with acute ReA after an infection with C pneumoniae are reported. Three had a symptomatic preceding upper respiratory tract infection and two had no such symptoms. In all patients a C pneumoniae-specific lymphocyte proliferation in synovial fluid and a high specific antibody titre suggesting an acute infection was found. CONCLUSION--C pneumoniae needs to be considered a new important cause of reactive arthritis.

 

Jim K Sat, 2008-10-04 10:12

CPn and other diseases

CPn and other diseases

Burden of infection and insulin resistance in healthy middle aged men This paper finds inflammation and infection related to blood glucose
Cpn in "wet" macular degeneration This article in the lay press details new findings that CPn is responsible for the inflammation seen in AMD. The abstract of the actual research is HERE

Behcets may be CPn related. A disease traditionally thought to be autoimmune is found to have significant titers of CPn.

-Cpn in prostate pathology This research found CPn in prostates with pathology. It even offers the theory that patholgy from hypertrophy to cancer represents different stages of infection.

-Chlamydia Pneumoniae in Interstitial Cystitis Is IC a mystery disease or is it a bacteria? This paper outlines the results of research investigating this.

Interstitial cystitis and CPn Link out to paper on this subject.

Chlamydia pneumoniae and Rosacea

mrhodes40 Sun, 2006-06-04 11:28

Chlamydia pneumoniae in human gingival cells

Chlamydia pneumoniae in human gingival cells
Int Immunopharmacol. 2008 Sep;8(9):1239-47. Epub 2008 May 22

Modulation of cytokine and beta-defensin 2 expressions in human gingival fibroblasts infected with Chlamydia pneumoniae.

Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Faculty of Medicine and Surgery -Second University of Naples, Naples, Italy.

Human beta-defensin 2 is an antimicrobial peptide that is produced by several epithelial cells after stimulation with micro-organisms and inflammatory mediators. Gram-negative bacteria, which are typically detected in periodontal pockets in periodontitis, elicit a stronger antibacterial peptide response of human beta-defensin 2 by epithelial cells. In this study, we investigated whether Chlamydia pneumoniae is able both to enter and grow in human gingival fibroblasts (HGF), to modify the production of cytokines, and is involved in regulation of beta-defensin 2 expression. Gingival fibroblasts discarded from periodontal procedures on healthy young individuals were infected with viable C. pneumoniae or with heat- or ultraviolet-inactivated organisms at a multiplicity of infection of 4 inclusion-forming units per cell. Our results demonstrate that after 48 h of incubation with viable C. pneumoniae, gingival fibroblasts showed a proliferative response as seen by both colorimetric assay and direct cell count (40% and 45%, respectively). Moreover, cells incubated with viable or ultraviolet light-inactivated C. pneumoniae organisms showed an increase in the levels of interleukin-6, interleukin-10 and human beta-defensin 2 in a time-dependent fashion, while the cells infected with heat-killed bacteria did not show a significant production either of the cytokines or beta-defensin 2 at any time. In conclusion, we demonstrate the correlation between multiplication of C. pneumoniae in human gingival fibroblasts and release of interleukin-6, interleukin-10 and up-regulation of beta-defensin 2, suggesting that gingival fibroblasts may be a periodontium niche for obligate intracellular C. pneumoniae and may play a role in innate gingival immune system and inflammatory response mechanisms of periodontitis.

Jim K Sat, 2008-07-12 23:50

Chlamydia pneumoniae infection results in generalized bone loss

Chlamydia pneumoniae infection results in generalized bone loss
 Microbes Infect. 2008 Jun 29. [Epub ahead of print]

Chlamydia pneumoniae infection results in generalized bone loss in mice.

Department of Molecular Biology, Umeå University, SE-90187, Umeå, Sweden.

Osteoporosis is associated with a general bone loss. Whether infections could contribute to osteoporosis is not known. Chlamydia pneumoniae causes chronic infections and produces potentially bone resorptive cytokines. The effect of C. pneumoniae infection was investigated in vivo in 10-week old mice (c57BL/6) and in vitro in the human osteoblast-like cell line hFOB 1.19 (hFOB). Bone mineral density (BMD) was measured before and 16 days after infection. C. pneumoniae-infected mice had decreased (p<0.05) total and subcortical BMD at the distal femur and proximal tibia compared with controls, but no body-weight gain differences. IL-6 (56 vs. 39pg/mL, p=0.02) and IL-1beta (11 vs. 0pg/mL, p=0.003) levels in sera, and CD3(+) T-cells (p=0.04) were higher in infected mice compared with controls. In vitro, hFOB infected with C. pneumoniae was associated with increased IL-6 (p=0.01) and RANKL (p<0.05) mRNA expression; additionally, IL-6 secretion increased in a dose-dependent manner (p<0.05). In summary, mice infected with C. pneumoniae had generalized bone loss associated with increased IL-6 and IL-1. In addition, C. pneumoniae established an infection in an osteoblast cell line in vitro with similar cytokine profiles as those in vivo, supporting a causal linkage.

Jim K Mon, 2008-07-28 23:49

Chlamydophila pneumoniae inhibits differentiation of progenitor adipose cells and impairs insulin signaling

Chlamydophila pneumoniae inhibits differentiation of progenitor adipose cells and impairs insulin signaling
 Cpn has been linked to obesity and weight gain, obviously an area of great interest. This is the first piece of research to reveal more about the possible mechanisms: inflammation (suprise, suprise) and impaired insulin signaling.
 
J Infect Dis. 2008 Feb 1;197(3):439-48.Links

Chlamydophila pneumoniae inhibits differentiation of progenitor adipose cells and impairs insulin signaling.

Toronto General Hospital Research Institute, Toronto, Ontario, Canada.

BACKGROUND: Recent clinical studies have shown Chlamydophila pneumoniae seropositivity to be related to overweight status and inversely related to insulin sensitivity. The present study was performed to investigate the potential effects of C. pneumoniae infection of adipocytes. METHODS: 3T3-L1 cells and primary epididymal preadipocytes were infected with C. pneumoniae either before or after induction of differentiation, and the effects on adipogenesis and insulin signaling were determined. Tumor necrosis factor (TNF)-alpha signaling was examined by assessing the effects of C. pneumoniae infection in preadipocytes isolated from epididymal adipose tissue of both wild-type and TNF-alpha(-/-) mice. RESULTS: C. pneumoniae successfully infected both undifferentiated and differentiated 3T3-L1 cells in vitro. The bacteria were also detected in adipose tissue of infected low-density lipoprotein receptor-deficient mice. TNF-alpha protein levels were significantly increased in cells infected with either live or heat-killed C. pneumoniae or treated with lipopolysaccharide or heat-shock protein 65; this increase was associated with inhibition of adipocyte differentiation and down-regulation of insulin-stimulated tyrosine-phosphorylated insulin receptor and its substrate. In contrast, C. pneumoniae infection in TNF-alpha(-/-) adipocytes produced no apparent changes, but addition of recombinant TNF-alpha reversed this effect. CONCLUSIONS: We demonstrate for the first time that C. pneumoniae can infect murine pre- and postdifferentiated adipocytes and, through a TNF-alpha-mediated inflammatory mechanism, can impair differentiation and insulin signaling.

Jim K Sun, 2008-04-06 13:05

Chronic Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral Diseases, Garth L. Nicolson, PhD

Chronic Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral Diseases, Garth L. Nicolson, PhD

This is a quite excellent review by Dr. Nicholson published in a mainstream peer reviewed scientific journal. He gathers together a considerable breadth of the research available on infectious sources of these diseases while being even handed in acknowledging the lack of scientific concensus and negative findings. Dr. Nicholson has been a leading researcher in the infectious paradigm for a number of illness, especially CFIDS and Gulf War syndrome.

 

Chronic Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral Diseases
Garth L. Nicolson, PhD(Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, CA)
LABMEDICINE

Jim K Mon, 2008-04-14 21:31

Chronic Fatigue Fibromyalgia Research

Chronic Fatigue Fibromyalgia Research

This is the research that we have relating Chlamydia pneumoniae to CFS and Fibromyalgia:

-Cpn in Chronic Fatigue -This work supports the above work in CFS and cryptic organisms. This time done by researchers in California.

-Infections and Fibromyalgia- If you are using or prescribing this treatment, please read this paper. It overviews the idea of infectious causes for chronic illness and is excellent.

mrhodes40 Sat, 2006-06-03 16:02

General Information Research Page

General Information Research Page

The General Information Page:

CPn Epidemiology Epidemiology means the study of how often and where a germ crops up.

Early events in CPn infection of host cells Short pubmed abstract.

Pharmacodynamics of Antichlamydials This paper addresses the issues of various lifecycles and pharmacodynamics. It is very clear that various agents are needed to eradicate CPn. Link out. Whole citation.

Chlamydiae.com link This site has tremendous technical information about CPn

Slides for a powerpoint slide presentation by Charles Stratton on Cpn.

Chlamydia pneumoniae: crossing the barriers? This long paper is included in totality. It addresses the issue of how CPn crosses epithelial barriers, causes inflammation and how it invades and parasitizes cells. A must read for the physician contemplating using this approach. Provides background.

Research by Charles Stratton and co-researchers This is a simple list of the finished work, includes a link to a complete list. Much of this relates to MS.

Cpn in chronic diseases This is a link out to work that overviews the main issues in CPn in chronic illness. A must read for the serious investigator.

Preliminary report on Wheldon/Stratton case studies This report outlines the theory and usefulness of metronidazole being added to the CPn protocol.

Persistent Chlamydial Envelope antigens This paper describes finding that chlamydia trachomatis can continue to induce inflammation well after treatment. This indicates that persistence of inflammation may well be a feature of CPn infection.

Review: Bacterial host Interactions This review of material relating to bacteria and how persistent infections may be supported by faulty mechanisms inside the idividual body is a must read. Somehwat technical, it's in depth look at the current research regarding this subject is essential for understanding that persistence is well recognized even if clarity about just exactly how it happens is just beginning.

Potential Role of Infections in Chronic Inflammatory Disease This self explanatory title names a referenced opinion paper written by a medical researcher and professor. It is a PDF file.

mrhodes40 Sat, 2006-06-03 15:58

Interesting Article: FIR Sauna improves pulmonary hyptertension in patients with COPD

Red

Another recent interesting article on FIR Sauna, this time suggesting that it improves pulmonary hypertension in patients with COPD:

J Cardiol. 2008 Apr;51(2):106-13. Links

Repeated waon therapy improves pulmonary hypertension during exercise in patients with severe chronic obstructive pulmonary disease.

Umehara M, Yamaguchi A, Itakura S, Suenaga M, Sakaki Y, Nakashiki K, Miyata M, Tei C.

Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduated School of Medicine, Kagoshima University, Sakuragaoka 8-35-1, Kagoshima 890-8520, Japan.

OBJECTIVES: Repeated Waon therapy, which uses a far infrared-ray dry sauna system, improved the vascular endothelial function and the cardiac function in patients with chronic heart failure. In patients with chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH) is associated with a poor prognosis. We investigated whether repeated Waon therapy improves PH, cardiac function, exercise tolerance, and the quality of life (QOL) in patients with COPD. METHODS: Consecutive 13 patients with COPD, who met the Global Initiative for Chronic Obstructive Lung Disease criteria and had breathlessness despite receiving conventional treatments, were recruited for this study. They underwent Waon therapy at 60 degrees C in sauna for 15 min following 30 min warmth with blankets outside of the sauna room. This therapy was performed once a day, for 4 weeks. Cardiac function, exercise tolerance, and St. George's Respiratory Questionnaire (SGRQ) were assessed before and 4 weeks after Waon therapy. RESULTS: Right ventricular positive dP/dt at rest elevated significantly from 397 +/- 266 to 512 +/- 320 mmHg/s (p = 0.024) after the therapy. While the PH at rest did not significantly decrease, the PH during exercise decreased significantly from 64 +/- 18 to 51 +/- 13 mmHg (p = 0.028) after Waon therapy. Furthermore, the therapy prolonged the mean exercise time of the constant load of cycle ergometer exercise test from 360 +/- 107 to 392 +/- 97 s (p = 0.032). The total scores of SGRQ improved from 59.7 +/- 16.9 to 55.3 +/- 17.2 (p = 0.002). In addition, no adverse effects were observed related to Waon therapy. CONCLUSIONS: Repeated Waon therapy improved right ventricular positive dP/dt, PH during exercise, exercise tolerance and the QOL in patients with severe COPD.

 

 

Lab analysis of CPn

Lab analysis of CPn

PCR analysis of CPN This technical paper is a must for the professional and interested techies. How can it be some say it's there and other researcher say it's not? The answer is here.

-Results, and Clinical Performance of Five PCR Assays for Detecting Chlamydia pneumoniae DNA in Peripheral Blood Mononuclear Cells A must read for the interested person interested in the technical details of finding these cryptic bacteria. You must understand this if the research that is done using other tests which find no relationship to CPn is to be properly understood.

Comparison of Five Serologic Tests for Diagnosis of Acute Infections by Chlamydia pneumoniae Another page with 5 tests being compared this one from 2000. Full citation available.

mrhodes40 Sat, 2006-06-03 16:35

Multiple Sclerosis Research

Multiple Sclerosis Research

MS is covered in this page. Please read more from the other research pages also as it is the whole picture that makes it compelling not just what is here....

A review of PCR in CPn infection by David WheldonThere are many studies on MS using the PCR to look for CPn. this review by David Wheldon is insightful

Chlamydia Pneumoniae infection in Neuronal cells lines

CPn respiratory infection associated with relapse in MS

Annotation by Marie with links on nitric oxide CPn and MS

Nitric Oxide and CPn: Multiple sclerosis link?

CPn infection induces transmigration of monocytes through human brain epithelial cells This work was undertaken to see if CPn might transmigrate because there is some work associating CPn with AD. Once you see that it can migrate across the BBB and that it can infet microglia and brain cells, is it such a leap to imagine it could cause MS?

Detection of chlamydial bodies and antigens in the central nervous system of patients with multiple sclerosis The newest published research on CPn in MS released October 1 2005. This work used several methods for detection of CPn in these MS patients, proving this work to be very thorough and extremely convincing. Many others have "tried" to find CPn using one method such as PCR, but his work also reaffirmed the assertion that CPn was present with other approaches as well.

-Pilot study to examine the effect of antibiotics on MRI outcomes in RRMS This is the most recent research to read if you are interested in MS and CPn. This study was small but it highlights interesting points about the reaction of the MS brain to antibiotic treatment.

The clinical response to minocycline in multiple sclerosis is accompanied by beneficial immune changes: a pilot study. This study was looking at minocin as an imunomodulatory agent but the positve responses in terms of gad enhancing lesions and relapses makes a person consider that there is likely more than one reason to do CAPs.

-Assoc. of Chlamydia pneumonie with nervous sytem disease This paper is a must read if you have MS.

Chlamydia pneumoniae infection of microglial cells Very important paper. Please read.

CSF molecular demonstration of CPn DNA is associated with cinical and brain magnetic resonance in RRMS This paper from 2004 shows that several neurolgoical diseases are associated with evidence of CPn in the brain, but also indicates that active disease of MS has a higher association. Importantly taken with Balin's work on AD we are beginning to see a neurological pathogen that possibly causes several kinds of brain pathologies. Since we know other germs like staph has the same kind of differing presentations, is that really so odd?

Epidemiologic Evidence for MS as an infection- J F Kurtzke Classic important paper. Kurtzke is clear that an infectious agent is to blame for MS. This in depth report includes an immene amount of data on the Faroese.

mrhodes40 Sat, 2006-06-03 16:07

Bacterial Genomics Reveals MS Trigger

Infection with a common bacteria could be the switch that turns on the autoimmune response in multiple sclerosis (MS) according to the findings of Wayne State University PhD graduate, Derek Lenz, now of the Scripps Research Institute in La Jolla, Calif. He described the work he carried out as part of Robert Swanborg’s team at Wayne State University School of Medicine. He said studies in rats show that an antigen found in the bacteria Chlamydia pneumoniae mimics part of a myelin protein in the animal’s central nervous system. When injected into the animal, it provokes the immune response that causes the rodent version of MS, experimental allergic encephalitis.

 http://tinyurl.com/8ckw6 

 

You GO, Derek Lenz! Thanks for finding this Jeanneroz. I am SO going to enjoy re-educating that young neuro I fired three years ago!

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Well of course we knew this here, but isn't it great to have ones beliefs validated, yet again.

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

Jeanneroz, could you cut and past the full link out in view then add a space to it and it may work for me.  I cannot access the article throught the link mechanism that you provided.  Thanks for sharing.  Louise
  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

A doctor who does his homework, good deal. More doctors should be a little more curious about their profession and read up on stuff like this. We the patient shouldnt have to be the initiater.

Fibro, CFS,  Myco, CPN, Stratton protocol, Zithro 500mg M/W/F/S, Doxy 100mg 2x day, NAC 1200mg 2x day, Flagyl and INH 2 week pulses 400 mg 3x day, Rifampin, 300mg 2x day,  Still cant shake it but improving.

Yet, we are the initiators and have been for a very long time.Thank goodness, we are not alone and have the brilliant questioning that makes this site so unique.

Educating neuros is a good idea if one can bear hearing the negativity aimed at all of us.

Everyone here, man or woman -  YOU GO!!!!!!

Happy 2009. I am with all of you, in spirit, hopes and desires.

Loulou

diagnosed MS Jan.2000 ,  chronic neurological lyme disease Nov.2002.

doxy 100 mg. 1BID. roxy.150 mg.? BID,adding rifampin soon, pulsed tini. every 3 weeks, as of oct.17/08, rifampin,naltrexone (LDN),NAC, nystatin, major wheldon supplemrnts daily,

Season's greetings everyone, but has anyone noticed that this link from Wayne State University is six years old?.............Sarah

An Itinerary in Light and Shadow

Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

I didn't really think it mattered... but don't you find it interesting that 6 YEARS AGO they made the possible connection??

 

JeanneRoz ~ DX'd w/ CPN 4/2007; 6/07 -"officially" dx'd w/CFIDS/FM; also: HHV6, EBV, IBS-C, 100 Doxy:BID; 500 mg Biaxin BID; Tindamax Pulses, B12 shots, ERFA Dessicated Thyroid,Cortef, Iodoral 25 mg, Vit D-6,000 uni

Wayne State has been doing work of this sort for many years.Dr. Lida Mattman , recently deceased, virologist, etc. penned the medical book Stealth Pathogens in the 80s out of Wayne State. Originally  professor emeritus from Yale - a brilliant woman and ahead of her time.

So we all should pay attention.

Loulou

diagnosed MS Jan.2000 ,  chronic neurological lyme disease Nov.2002.

doxy 100 mg. 1BID. roxy.150 mg.? BID,adding rifampin soon, pulsed tini. every 3 weeks, as of oct.17/08, rifampin,naltrexone (LDN),NAC, nystatin, major wheldon supplemrnts daily,

Actually, as I read it, cpn is here considered a trigger for the AUTO-IMMUNE disease of ms. That's a possibility that we have not ruled out but, as I understand it, we do not generally consider MS an auto-immune disease. Am I wrong?

PPMS-misdiagnosed 2001-diagnosed 2006. Probably caught cpn in birth canal but it didn't pass BBB until my 40s. Minocycline 7 mos.- resulting bronchitis 5 months.Go to private m.d. out-of-plan. Wheldon CAP 3/2/07 Stopped 12/12; resumed 12/13

Autoimmune or not?????????????That is the pervasive question..................Some neuros say yes autoimmune, others say no...

Dr. Wheldons protocol gives us some hope..The rest are merely names - I keep going.What else is there??

LOULOU

diagnosed MS Jan.2000 ,  chronic neurological lyme disease Nov.2002.

doxy 100 mg. 1BID. roxy.150 mg.? BID,adding rifampin soon, pulsed tini. every 3 weeks, as of oct.17/08, rifampin,naltrexone (LDN),NAC, nystatin, major wheldon supplemrnts daily,

Sorry, everyone, but I didn't think anyone had noticed the date.  This is old news and DW was corresponding with Hudson years ago.  I thought it was sad that things had changed so little since then................Sarah

An Itinerary in Light and Shadow

Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

It is definitely sad. Thank you DW .

Things in medicine are profoundly slow.Sarah, I'm sure you know more about the inner circles of the med. system than most?

This, so to speak, hierarchy makes us so aware that pharmaceutical companies appear to unfortunately govern medicine and  the "practice" of it.eg. no cause, no cure, bacterial, viral, and the list goes on and on.....

Forget the politics as much as possible. Do what you can . Exercise, go outside (weather permitting), stay on CPN.....................

Loulou

I'm starting to sound political. Must be the times we're living in.

Happy 2009

diagnosed MS Jan.2000 ,  chronic neurological lyme disease Nov.2002.

doxy 100 mg. 1BID. roxy.150 mg.? BID,adding rifampin soon, pulsed tini. every 3 weeks, as of oct.17/08, rifampin,naltrexone (LDN),NAC, nystatin, major wheldon supplemrnts daily,

loulou - "Stay on cpn"????????   You are hereby banished from the punchbowl. Cpn=bad. ABX=good. Image removed.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

It is possible it is autoimmune and directly attacks tissue, HSP 60 maybe, and very likely genetic and environmental.  That is maybe why it has taken so long to tie everything together, many variables.

 

The body is very complex, it is very hard to experiment with people much less track them.  Medicine is very political.  All things to slow finding the cure.  Many very fine doctors now are on the germs trail, it will get a lot harder for it to do damage as before.

Cpn, Mycoplasma, Chronic EBV, M.S.(MRI, Spinal Tap-greater than 5 oligoclonal bands and VEP), PANDAS(OCD). Wheldon CAP (started 12/08), Azithromycin/Clarithromycin(12/09), Lithium, Lamictal, NAC(2.4g/day), D3(15,000IU/day)

Whoops! Confused for a change.....................not cpn    YES cap, YES antis.

Thanks Mac for pointing that out- I missed it.

Loulou

diagnosed MS Jan.2000 ,  chronic neurological lyme disease Nov.2002.

doxy 100 mg. 1BID. roxy.150 mg.? BID,adding rifampin soon, pulsed tini. every 3 weeks, as of oct.17/08, rifampin,naltrexone (LDN),NAC, nystatin, major wheldon supplemrnts daily,

If Dr. Lida Mattman wrote the medical book "Stealth Pathogens" in the 80's, and was a Nobel Prize candidate because of it, then why in the world are so many having so much trouble finding doctors who will go along with this protocol, and why is there such a battle within the medical community?  I honestly and truly don't understand.

Kelly

Diagnosed FMS Feb '07.  2x/day: 600 mg NAC, 100 mg Doxy, 500 mg Amoxicillin, 2000 iu Vit. D.  450 mg Valcyte.  250 mg Azi M/W/F.  500 mg 375 mg Flagyl pulses every 3-4 weeks.  Started CAP June '07. 

I  wish I knew a solid unbiased answer to your valid questions.

Get involved with ILADS. mORE INFO THat ,as me, will make you more aware, however, add to your confusion. Hoping this baffling info will stop, once and for all BUT I bet it doesn't!!

Happy 2009

Loulou

ps Let it suffice to inform you that Dr. Mattman was hidden, literally, for her beliefs, almost thrown in jail, etc.etc. I stayed with her close to the end of her proud,informative life. I learned a lot from her.

diagnosed MS Jan.2000 ,  chronic neurological lyme disease Nov.2002.

doxy 100 mg. 1BID. roxy.150 mg.? BID,adding rifampin soon, pulsed tini. every 3 weeks, as of oct.17/08, rifampin,naltrexone (LDN),NAC, nystatin, major wheldon supplemrnts daily,

Wow, LouLou - where was Erin Brockovich during all of this?!  Dr. Mattman's story sounds fascinating - it would be great to see a book written about her life!  She really was the pioneer, wasn't she?  So sad that she was also a pioneer for those persecuted for daring to have evidence that contradicts those who hold the power.

Kelly

Diagnosed FMS Feb '07.  2x/day: 600 mg NAC, 100 mg Doxy, 500 mg Amoxicillin, 2000 iu Vit. D.  450 mg Valcyte.  250 mg Azi M/W/F.  500 mg 375 mg Flagyl pulses every 3-4 weeks.  Started CAP June '07. 

Chlamydia pneumoniae-specific intrathecal oligoclonal antibody response predominantly detected in subset of multiple sclerosis

Chlamydia pneumoniae-specific intrathecal oligoclonal antibody response predominantly detected in subset of multiple sclerosis

J Neurovirol. 2010 Jan 6. [Epub ahead of print]

Chlamydia pneumoniae-specific intrathecal oligoclonal antibody response is predominantly detected in a subset of multiple sclerosis patients with progressive forms.

Fainardi E, Castellazzi M, Tamborino C, Seraceni S, Tola MR, Granieri E, Contini C.

Neuroradiology Unit, Department of Neurosciences and Rehabilitation, Azienda Ospedaliera-Universitaria, Arcispedale S. Anna, Ferrara, Italy.

The purpose of this study was to verify the actual involvement of Chlamydia pneumoniae in multiple sclerosis (MS) by the evaluation of its specific intrathecal humoral immune response in MS. We measured by enzyme-linked immunosorbent assay (ELISA) technique cerebrospinal fluid (CSF) and serum levels of anti-C. pneumoniae immunoglobulin G (IgG) in 27 relapsing-remitting (RR), 9 secondary progressive (SP), and 5 primary progressive (PP) MS patients, grouped according to clinical and magnetic resonance imaging (MRI) evidence of disease activity. Twenty-one patients with other inflammatory neurological disorders (OIND) and 21 with noninflammatory neurological disorders (NIND) were used as controls. Quantitative intrathecal synthesis of anti-C. pneumoniae IgG was determined by antibody-specific index (ASI), whereas the presence of C. pneumoniae-specific CSF oligoclonal IgG bands was assessed by antigen-specific immunoblotting. ASI values indicative of C. pneumoniae-specific intrathecal IgG synthesis were present in a small proportion of MS (29.3%), OIND (33.3%), and NIND (4.8%) patients and were significantly more frequent (P < .05) in total MS and in OIND than in NIND and in SP (P < .01) and PP MS (P < .05) than in RR MS. C. pneumoniae-specific CSF-restricted OCB were detected only in three SP, one PP, and one RR MS patients. These findings suggest that an intrathecal production of anti-C. pneumoniae IgG is part of humoral polyreactivity driven by MS chronic brain inflammation. However, an intrathecal release of C. pneumoniae-specific oligoclonal IgG can occur in a subset of patients with MS progressive forms in whom a C. pneumoniae-persistent brain infection may play a pathogenetic role.

 

http://www.ncbi.nlm.nih.gov/pubmed/20053141?itool=Email.EmailReport.Pub…

Jim K Sat, 2010-01-09 14:39

Cpn DNA and mRNA in PMBC's and CSF of patients with multiple sclerosis.

Neurosci Res. 2008 Sep;62(1):58-61. Epub 2008 May 20.

Chlamydophila pneumoniae DNA and mRNA transcript levels in peripheral blood mononuclear cells and cerebrospinal fluid of patients with multiple sclerosis.

Section of Infectious Diseases, Department of Clinical and Experimental Medicine, University of Ferrara, Ferrara, Italy. cnc@unife.it

Chlamydophila pneumoniae DNA and mRNA transcripts were investigated by PCR and RT-PCR in fresh CSF and PBMC specimens co-cultured in Hep-2 cell lines and collected from 14 patients with definite RR MS and 19 patients with other inflammatory (OIND) and non-inflammatory (NIND) neurological controls. A positivity for C. pneumoniae DNA and mRNA was detected in CSF and PBMCs of 9 RR MS patients (64.2%) with evidence of disease activity, whereas only 3 controls were positive for Chlamydial DNA. These preliminary findings suggest that C. pneumoniae may occur in a persistent and metabolically active state at both peripheral and intrathecal levels in MS, but not in OIND and NIND.

Molecular detection of Parachlamydia-like organisms in cerebrospinal fluid of patients with multiple sclerosis.

Mult Scler. 2008 May;14(4):564-6

Molecular detection of Parachlamydia-like organisms in cerebrospinal fluid of patients with multiple sclerosis.

Section of Infectious Diseases, Department of Clinical and Experimental Medicine, University of Ferrara, Ferrara, Italy. cnc@unife.it

The presence of Chlamydia-like organism DNA was investigated by polymerase chain reaction (PCR) in cerebrospinal fluid (CSF) samples from 27 patients previously found positive for Chlamydia pneumoniae DNA: 12 with multiple sclerosis (MS), grouped according to clinical and magnetic resonance imaging (MRI) evidence of disease activity, 8 with other inflammatory neurological disorders and 7 with non-inflammatory neurological disorders. PCR evidence of Chlamydia-like organisms in CSF was observed only in two relapsing-remitting MS patients with clinical and MRI disease activity. These findings suggest a possible association between C. pneumoniae and Chlamydia-like organism brain infections as a cofactor in MS development.

THANKS JimK

we know that!!  Glad some research is being done, that is excellent.

peace

r

 

CFIDS/ME, FMS, MCS, IBS, EBV, CMV, Cpn, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplements+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyl/day-5 days<

Respiratory issue and Chlamydia Pneumoniae

Respiratory issue and Chlamydia Pneumoniae

Asthma and Infections,

Seroprevalence of CPn infections in otolaryngeal infections

Mechanisms of chlamydiophilia mediated GM-CSF release in HUman Bronchial cellsHow does CPn tirgger inflammatoin in lung tissue? this attempts to pinpoint the answer

Serum IgG and IgA antibodies to CPn in EmphysemaThis article indicates that serology is positive in emphysema and that clinical course and worsening is tied to CPn status

Asthma and CPn. Explains interaction of patient immune system with the CPn. Technical.

-Cpn in recurrent respiratory infections This work with children with recurrent respiratory infections indicates that treating for cryptic bacteria improves outcomes. Treatment was prolonged due to the nature of cryptic, or "atypical" bacteria.

Chlamydia Pneumoniae and COPD This reserach indicates that acute exacerbations of COPD re associated with CPn.

-Cpn in asthma This research indicates that cryptic bacteria play a role in asthma. Outcomes were improved by adding abx.

mrhodes40 Sat, 2006-06-03 16:26

Severe asthma exacerbation: role of acute Cpn & Mycoplasma

Severe asthma exacerbation: role of acute Cpn & Mycoplasma
1: Respir Res. 2008 May 30;9:48.

Severe asthma exacerbation: role of acute Chlamydophila pneumoniae and Mycoplasma pneumoniae infection.

Emergency Medicine Department, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Gruppo NIV Policlinico, Milan, Italy. r.cosentini@gmail.com

BACKGROUND: Chlamydophila pneumoniae and Mycoplasma pneumoniae are associated with acute exacerbation of bronchial asthma (AEBA). The aim of this study was to evaluate the correlation between these acute bacterial infections and the severity of AEBA. METHODS: We prospectively analysed consecutive patients admitted to the Emergency Department with acute asthma exacerbation. In every patient peak expiratory flow (PEF) measurement was performed on admission, and spirometry during follow-up. Serology for Chlamydophila and Mycoplasma pneumoniae was performed on admission and after 4-8 weeks. RESULTS: Fifty-eight patients completed the study. Acute atypical infections (AAI) was observed in 22/58 cases; we found single acute C. pneumoniae in 19 cases, single acute M. pneumoniae in 2 cases, and double acute infection in one case. Functional impairment on admission was greater in patients with AAI than in patients without AAI (PEF 205 +/- 104 L/min vs 276 +/- 117 p = 0.02) and persisted until visit 2 (FEV1% 76.30 +/- 24.54 vs FEV1% 92.91 +/- 13.89, p = 0.002). Moreover, the proportion of patients who presented with severe AEBA was significantly greater in the group with AAI than in the group without AAI (15/22 vs 12/36, p = 0.01; OR 4.29, 95% CI 1.38-13.32). CONCLUSION: Our data suggest an association between acute atypical infection and a more severe AEBA.

Jim K Mon, 2008-07-28 23:56

The Cardiac Research Links

The Cardiac Research Links

CPn and Cardiovascular Issues -

Statins and CPn

Persistent CPn infection of cardiomyocytes associated with acute MI

Atherothrobotic events and CPn Long term study on CPn IgG and IgA findings in atherothrombosis

Higher incidence of persistent chronic infection of Chlamydia pneumoniae among coronary artery disease patients in India is a cause of concern.

CPn and atherosclerosis Article which is in depth and includes many interesting diagrams and pictures. An overview of the understanding of the role CPn plays in cardiovascular issues with many links in the work

Experimental Chlamydia pneumoniae infection model: effects of repeated inoculations and treatment This article is about mice repeatedly infected with CPn and the impact on the cardiovascular system. luteolin in mentioned.

The role of endothelial dysfunction and Chlamydia pneumoniae infection in patients with ischemic stroke Intimal thickness is a measure of atherosclerosis this research correlates it with CPn seropositivity

Cpn in heart disease Think all this research is done by one or two people? Not at all. This link out highlights work done in Seattle on several cryptic organisms in CFS.

Doxycycline use and incidence of CAD This retrospective study of clients in a Greek cardiac practice reviewed use of doxy and later incidence of CAD. A reduction was seen.

The CDC on CPn The centers for disease control recognizes CPn as an emerging issue in atherosclerosis and other diseases. Once again CPn is becoming more recognized in chronic illness traditionally thought "autoimmune"

The Influence of CPn on aortic stiffness in healthy young menIs CRP a response to CPn in cardiovascular issues? C reactive protein and pulse wave velocity measurement of stiffness were both statistically higher in the IgA positive group for CPn.

Antibodies to 60-kilodalton heat shock protein and outer membrane CPn in people with CAD (coronary artery disease) Again, if you have CAD you have antibodies to the various proteins of CPn.

Autoimmunity to human heat shock protein 60, CPn infection, and inflammation in predicting coronary artery riskAutoimmunity plays a role in CPn infection

Antibody respose to Chlamydial heat shock protein strongly associated with cornoary artery disease HSP's are a contributing factor in CPn disease in study after study.

Serological evidence of CPn LPS antibodies in atherosclerosis of various vascular regions There are several proteins associated with CPn tht are immunogenic.

Chronic CPn infection associated with serum lipid profile known to be a risk for CAD CAD is coronary artery disease

Elevated antibody levels against Chlamydia pneumoniae, human HSP60 and mycobacterial HSP65 are independent risk factors in myocardial infarction and ischaemic heart disease. How have we missed this for so long?

Synergistic effect of persistent Chlamydia pneumoniae infection, autoimmunity, and inflammation on coronary risk. Several factors at work accounting for the research into other risk factors.


Chlamydial and human heat shock protein 60 homologues in acute coronary syndromes. (Auto-)immune reactions as a link

Effect of chronic Chlamydia infection with non-specific inflammation on cardiovascular complications in acute myocardial infarct

Azithromycin for the secondary prevention of coronary events Azithromycin alone, a bacteriostatic agent, is incapable of ridding the body of CPn. The EB's are not touched by this drug, the cryptic and peristant forms are encouraged, and it's bacteriostatic nature means the bacteria simply stop actively replicating and metabolizing until the coast is clear. You cannot create any meaningful research into this subject until you account for all lifecycle forms. We are essentially dealing with a form of resistance here. The conclusion of this study was that azith did not decrease coronary events.

Effect of prolonged treatment with azithromycin, clarithromycin, or levofloxacin on Chlamydia pneumoniae in a continuous-infection model This paper finds that treatment with standard chlamydia effective antibiotics does not eradicate persistence. This highlights the need for combination and very long term treatment if one wishes to eradicate CPn.

Azithromycin therapy in patients with chronic Chlamydia pneumoniae infection and coronary heart disease: immediate and long-term This one indicated a possibly positive outcome on fibrinolysis though again the azith did not impact CPn positivity. Taken with the abstract above we have a situation that is confusing to the clinician - until you understand the pathogen and it's lifecycle. Then these studies are clearly incomplete and therefore inconclusive.

The final report on the ROXIS study This paper outlines the ROXIS study on roxithromycin use in patients who had experienced an acute non q wave coronary problem. The folow up reposts a positive effect. This links to the whole citation.

Effect of Treatment for Chlamydia pneumoniae and Helicobacter pylori on Markers of Inflammation and Cardiac Events in Patients With Acute Coronary Syndromes
Another antibiotic study with positive results though serologic markers of CPn and H pylori were not affected by treatement. It might be suggested this means it was some other aspect of the abx that influenced the disease (ie antiinflammatory) but since persistent CPn is not reflected in serologic markers it is likely moot. The whole citation is linked here.

Heat-shock protein 60-reactive CD4+CD28null T cells in patients with acute coronary syndromes We can certainly recognize how that crafty CD4+CD28 combo from MS shows up in this cardiac study and also in RA, somehow researchers from different fields don't seem to recognize them yet as possibly caused by the same source CPn, not autoimmunity.

Fulminant carditis and CPn This is a case of carditis that turned out to be CPn and CP together.

mrhodes40 Mon, 2005-10-17 20:31

Vitamin D Abstracts & Commentaries

Vitamin D Abstracts & Commentaries Jim K Mon, 2008-04-07 22:46

Vieth Slide Show on Vitamin D- see this one if nothing else

Vieth Slide Show on Vitamin D- see this one if nothing else

The charts alone make it crystal clear: lack of sun exposure, low D levels and a host of diseases result. Critical for all of us living in northern climates, but especially true for people of African descent with dark skin. It's apparent from his presentation that even 2000 units a day is not enough for the elderly, African Americans, and those of us with illness. 4000 units a day is more like it.

http://wildhorse.insinc.com/directms13oct2005/

 

Jim K Fri, 2008-10-31 07:44

Another good article on Vit D3 & Autoimmune Disease

Red


Just ran across this fairly easy to read recent review article on Vit D3 and thought others might be interested:

The Complex Role of Vitamin D in Autoimmune Diseases

It's well worth a read...

 

Thanks Red!  Can't wait to read it.  :o)

Big hugs!

TP 

 

--

May 2008. NACx1200mg, D3x2000mg, B12x1000mcg. Allergies, chronic inflamation, eczema, long-term steroid use, sinusitis/cysts, BL/TN, FM, CF, arthritis, rosacea.

Corinna | GFA. Wheldon Protocol: 4–8/08. Can't kill the yeast.

Red

You're welcome, TP!   How are you doing so far?

On Combined Antibiotic Protocol for Cpn in Rosacea 01/06 - 07/07, On Vit D3 + NAC since 07/07 and daily FIR Sauna since 08/07

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

I am having more bad days than good ones but I am convincing myself that this is somehow a good thing... I think my pancreas is unhappy because it hurts (??) My old Edmonton MD is considering taking this on with me...YIPPEE!!! Ahem, I'm mean I feel cautiously optimistic.  Image removed.

First thing he told me to do was up the Vitamin D to 6000/day.  That's a good sign!

--

May 2008. NACx1200mg, D3x2000mg, B12x1000mcg. Allergies, chronic inflamation, eczema, long-term steroid use, sinusitis/cysts, BL/TN, FM, CF, arthritis, rosacea.

Corinna | GFA. Wheldon Protocol: 4–8/08. Can't kill the yeast.

Red

Too funny!   Glad to hear you're so cautiously optimistic!

Sorry to hear you're having more bad days than good, but this is really par for the course in the early days.  Still, remember attack the secondary porphyria with all options.  This is your big chance to pig out on those starchy carbs and glucose tabs with no guilt!

Keep us posted, and good luck with your Edmonton doc!  I like his advice on the Vit D3 btw.   In addition to its likely killing effects on Cpn, through the elevation of cathelicidins, it kills so many other pathogens that are likely involved as co-pathogens in many of our diseases/conditions.   I think it has been very instrumental in my own recovery.

But be careful about upping it too fast.   I can cause pretty heavy die-off and secondary porphyria symptoms itself...

 

On Combined Antibiotic Protocol for Cpn in Rosacea 01/06 - 07/07, On Vit D3 + NAC since 07/07 and daily FIR Sauna since 08/07

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Thanks Red. I've jumped to 4000 which may explain the way I'm feeling. I'm up to 2400 mg NAC now too.

I really appreciate your guidance!

Big hugs!
TP

--

May 2008. NACx2400mg, D3x4000mg, B12x1000mcg. Allergies, chronic inflamation, eczema, long-term steroid use, sinusitis/cysts, BL/TN, FM, CF, arthritis, rosacea.

Corinna | GFA. Wheldon Protocol: 4–8/08. Can't kill the yeast.

Red

That will definitely do it! Don't underestimate the power of the D...

As long as you don't have any medical reason not to, and I know this is counter to everything you've probably read up to this point about what you should do for good health, but definitely give glucose tabs a good try too. You can get them at any drugstore down here. I'm assuming it's the same up in your area:

http://www.drugstore.com/products/prod.asp?pid=37594&catid=10017

Take 2 or 3 and see if you don't feel a bit better in @ 20 minutes or so. If not, take another 2 or 3 to see if this works. If it does, you're likely suffering from secondary porphyria and should probably take glucose more regularly during the day to help minimize this problem. Others find the glucose based "Smarties" work too, and are cheaper. I seemed to notice more stomach irritation with them. Not sure why. Maybe it was the amount of citric acid. Anyway, glucose really helped earlier in treatment for me, and seems to really help others too...

I know you're probably worried about Candida, etc, but the cathelicidins elevated by Vit D3 have been shown to be pretty effective at killing Candida so do the glucose.  It may allow you to ramp up the Vit D3 more quickly...

Hope this helps. Keep us posted on your progress. I hope you feel better soon!

Big hugs back at you...

On Combined Antibiotic Protocol for Cpn in Rosacea 01/06 - 07/07, On Vit D3 + NAC since 07/07 and daily FIR Sauna since 08/07

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Thanks Red!

I admit to forgetting about the glucose when I feel this way. My head's not connected to this all just yet. I will pick up the glucose tomorrow, the local pharm had set some aside for me a while back and I've let myself get sidetracked.

I'm not going to worry about the candida issues while taking this on, unless/until I have to. I will post on my blog with updates, sorry to derail this one...Image removed.

Best wishes,
TP

 

--

May 2008. NACx2400mg, D3x4000mg, B12x1000mcg. Allergies, chronic inflamation, eczema, long-term steroid use, sinusitis/cysts, BL/TN, FM, CF, arthritis, rosacea.

Corinna | GFA. Wheldon Protocol: 4–8/08. Can't kill the yeast.

A superb review article, and a great find. Thanks Red! 

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Currently: 300mg BID Roxithromycin, Bactrim DS 2x/day, Tini 1000mg/day pulses; Vit D2000 units, T4 & T3

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Red

You're welcome, Jim.

TP, no worries about derailing this thread. You haven't...

The whole not thinking straight thing seems to be related to the secondary porphyria. The worse the secondary porphyria gets, the less reasoning you're able to muster.

If you have some sugar cookies on hand still, eat a couple tonight. They'll help you feel better. A caffeine-free sugary soda will even do.

Hang in there...

On Combined Antibiotic Protocol for Cpn in Rosacea 01/06 - 07/07, On Vit D3 + NAC since 07/07 and daily FIR Sauna since 08/07

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Are Influenza Epidemics a Result of Low Sunlight and Vitamin D?

Gotta love this one.

On the Epidemiology of Influenza - Source: Virology Journal, Feb 2008

by John J Cannell, et al.
October 12, 2008

[Note: the full text of this open-access article, outlining evidence that sun/vitamin D status could have "profound implications for the prevention of influenza" is available free at http://www.virologyj.com/content/5/1/29 ]

The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, "seemingly unmindful of traditional infectious disease behavioral patterns."

Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify – and attempt to explain – nine influenza conundrums:

1. Why is influenza both seasonal and ubiquitous and where is the virus between epidemics?

2. Why are the epidemics so explosive?

3. Why do they end so abruptly?

4. What explains the frequent coincidental timing of epidemics in countries of similar latitude?

5. Why is the serial interval obscure?

6. Why is the secondary attack rate so low?

7. Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?

8. Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers?

9. Why has influenza mortality of the aged not declined as their vaccination rates increased?

We review recent discoveries about vitamin D's effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies.

We hypothesize that two factors explain the nine conundrums:

• Vitamin D's seasonal and population effects on innate immunity,

•And the presence of a subpopulation of "good infectors."

If true, our revision of Edgar Hope-Simpson's theory has profound implications for the prevention of influenza.

Source: Virology Journal, Feb 2008, 5:29; DOI:10.1186/1743-422X-5-29 by Cannell JJ, Zasloff M, Garland CF, Scragg R, Giovannucci E. Department of Psychiatry, Atascadero State Hospital, California; Departments of Surgery and Pediatrics, Georgetown University, Washington, DC; Department of Family and Preventive Medicine, University of California San Diego, La Jolla, California; Department of Epidemiology and Biostatistics, University of Auckland, New Zealand; Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA.

 

This looks like a fantastic article. Not only from a vitamin D perspective, but also from an epidemiology/preventative-disease perspective. I'm probably abnormal, but I've been asking myself some of these questions for a long time. Finally some answers!

Thanks Jim.

garcia. 

 

Hunter: Don't think - experiment
Red

Great article, Jim.   Very intertesting read... Thanks!

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Re-reading it, I'm even more impressed with the findings. The charts alone on cold/flu reduction from only 2000 units of D during winter months are worth the read. Want to protect yourself from the next pandemic? Forget Tamiflu, get your D levels up!

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

D2 vs D3 supplementation: article link

D2 vs D3 supplementation: article link

Most prescription D is D2 rather than the more effective D3. This article has an excellent review of the state of the science and why D3 is preferred for supplementation.

http://www.ajcn.org/cgi/content/full/84/4/694

 

Jim K Wed, 2008-10-29 18:22

Detailed Info on Vitamin D, especially in relation to MP

Detailed Info on Vitamin D, especially in relation to MP

A lot of people coming to the site here have questions about the Marshall Protocol and the Cpn CAP, where we recommend Vitamin D supplementation in contrast to MP. The most detailed analysis of the MP in relation to what is known in the scientific literature about Vitamin D occurs in this link:

http://stuff.mit.edu/people/london/universe.htm

 

Jim K Mon, 2008-04-07 23:04

Interesting Study on Importance of Vitamin D3 for Proper Thyroid Function

Red

 

Since so many on the site are dealing with thyroid issues, I thought I'd pass this along...

First, here's a little news blurb on the study:

Modern Medicine: Vitamin D Directly Affects Thyroid Function in Mice

 

Below is the full study article.  While the article focuses on Graves' hyperthyroidism, the discussion and conclusion sections list some interesting findings of recent research on Vitamin D3's importance for proper thyroid function in general.   It's well worth a read:

Vitamin D deficiency modulates Graves' hyperthyroidism induced in BALB/c mice by thyrotropin receptor immunization.

 

Great find, Red. This might help make some sense over all the thyroid deficiency we see in CFIDS/ME from D deficiency compounded by infection, and certainly gives pause to pursuing a D deprivation model like the MP. Anyone here from the MP have resulting thyroid problems?

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Low Vitamin D Levels Linked to Chronic Pain in Women

Posting this one as a whole, seems "fair use" for an informational web site, because it includes a useful discussion of the limitations of the methodology of the study not found in the abstract. Still, it behooves those of us with pain to consider Vitamin D levels as at least a variable that either modulates pain itself or contributes to other factors, like infection, that generate pain and inflammation.

 Low Vitamin D Levels Linked to Chronic Pain in Women

Allison Gandey

Medscape Medical News 2008. © 2008 Medscape

August 18, 2008 — Women with low vitamin D levels have more chronic widespread pain, a new study has found. The modest findings do not support the use of vitamin D status as a key determinant for chronic pain, researchers suggest, but they do raise interesting questions about the possible influence of endocrine or immunological factors. The work is published online August 12 in the Annals of the Rheumatic Diseases.

Chronic widespread pain is thought to be a multifactorial condition. To date, the focus has been on psychosocial influences, note the study investigators, led by Kate Atherton, MD, from the University College London Institute of Child Health, in the United Kingdom. Although associations between chronic pain and general psychological distress, depression, somatization, and other factors have been consistently reported, translating these observations into management strategies has been fairly unsuccessful, they note.

Vitamin D deficiency has been suggested as a new modifiable risk factor for chronic pain. Vitamin D is a hormone precursor, which is obtained either through diet or skin synthesis. Using a nationwide population sample of white British adults, the researchers wanted to examine the link between vitamin D and chronic pain.

Women With Vitamin D Levels of 75 to 99 nmol/L Had Less Pain

"To our knowledge, this study is the largest population-based examination of the association between vitamin D status and chronic widespread pain to date," write the researchers. The work is also the first to consider related variations in lifestyle factors or to focus on white ethnic groups, they add.

The study included more than 9300 participants in England, Scotland, or Wales born during 1 week in March in 1958 who had completed a biomedical assessment at age 45 years. Of these, 6824 participants had data on 25-hydroxyvitamin D and pain.

Investigators found that chronic pain levels varied by 25-hydroxyvitamin D concentration in women, but not in men. "In our study, the lowest prevalence of chronic widespread pain was observed for women with 25-hydroxyvitamin D 75 to 99 nmol/L," Dr. Atherton and her team report. "This is intriguing given that 25-hydroxyvitamin D 75 nmol/L has been previously suggested as the cutoff point for optimal bone health."

Prevalence of Chronic Pain in Relation to Vitamin D Concentrations in Women

25-Hydroxyvitamin D (nmol/L) Women with Chronic Pain (%)
< 25 14.4
25 – 49 14.8
50 – 74 11.6
75 – 99 8.2
> 100 9.8

 

The investigators report there was an interaction between vitamin D concentration and sex in relation to chronic pain (interaction P = .006), which was not fully explained by differences in lifestyle or social factors (adjusted interaction P = .03).

The researchers point to a number of limitations of the work. They note the vitamin D status of participants was obtained during the study and may not represent the patient's status during the time that chronic pain developed, which may have been years earlier.

They also suggest that given the cross-sectional design of the study, it is not possible to establish whether suboptimal vitamin D status results in an increased risk for pain or whether changes in the behavior of subjects with pain result in reduced vitamin D concentrations.

"The lack of a stronger association between vitamin D and chronic pain in our general population sample may suggest that pain is primarily indicative of a severe vitamin D deficiency rather than a more gradual response to varying concentrations," the researchers write.

Dr. Atherton and her team report that it is unclear why an association between vitamin D and pain was observed in women but not in men. They suggest that since the women in the cohort are still mostly premenopausal, perhaps the influences of hormonal vitamin D on the regulation of estrogen activity may at least partly contribute to this sex difference.

"Nevertheless," they add, "given the observational nature of these data, we cannot exclude the possibility that our finding of an association between vitamin D status and chronic pain in women (or the lack of any association in men) is confounded by unmeasured factors.

"Follow-up studies are needed to evaluate whether higher vitamin D intake might have beneficial effects on [chronic widespread pain] risk," they conclude.

The researchers have disclosed no relevant financial relationships.

Ann Rheum Dis. Published online August 12, 2008. Abstract

Jim - And on the heels of your article

from the August 11, 2008, Archives of Internal Medicine (very reputable journal)

http://www.ncbi.nlm.nih.gov/pubmed/18695076

"Observational data suggests that low 25-hydroxyvitamin D levels (25[OH]D) are associated with diabetes mellitus, hypertension, and cancers. However, whether low serum 25(OH)D levels are associated with mortality in the general population is unknown. "

"the lowest quartile (25[OH]D levels <17.8 ng/mL) was associated with a 26% increased rate of all-cause mortality"

This is substantial by anyone's standards!

 

Daisy - Husband on CAP 5/07.  Husband died from Acute Myelogenous Leukemia Secondary to the Infusion of Novantrone.  Ie - the treatment with the conventional MS drugs killed him.

Daisy on her own CAP 11/2012. 

The evidense just keeps building up, doesn't it, what with Red's recent posts too.

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

More and more on Vitamin D

Following are some new Vitamin D abstracts by Holick. With 1,25-dihydroxyvitamin D involved in regulating more than 200 genes, you would think it might not be such a good idea to formulate treatment around Vitamin D starvation...
Jim

 Mol Aspects Med. 2008 Sep 2. [Epub ahead of print]Click here to read Links
    The vitamin D deficiency pandemic and consequences for nonskeletal health: Mechanisms of action.
    Holick MF.

    Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Vitamin D, Skin and Bone Research Laboratory, Boston University Medical Center, Boston, MA, United States.

    Vitamin D, the sunshine vitamin, is important for childhood bone health. Over the past two decades, it is now recognized that vitamin D not only is important for calcium metabolism and maintenance of bone health throughout life, but also plays an important role in reducing risk of many chronic diseases including type I diabetes, multiple sclerosis, rheumatoid arthritis, deadly cancers, heart disease and infectious diseases. How vitamin D is able to play such an important role in health is based on observation that all tissues and cells in the body have a vitamin D receptor, and, thus, respond to its active form 1,25-dihydroxyvitamin D. However, this did not explain how living at higher latitudes and being at risk of vitamin D deficiency increased risk of these deadly diseases since it was also known that the 1,25-dihydroxyvitamin D levels are normal or even elevated when a person is vitamin D insufficient. Moreover, increased intake of vitamin D or exposure to more sunlight will not induce the kidneys to produce more 1,25-dihydroxyvitamin D. The revelation that the colon, breast, prostate, macrophages and skin among other organs have the enzymatic machinery to produce 1,25-dihydroxyvitamin D provides further insight as to how vitamin D plays such an essential role for overall health and well being. This review will put into perspective many of the new biologic actions of vitamin D and on how 1,25-dihydroxyvitamin D is able to regulate directly or indirectly more than 200 different genes that are responsible for a wide variety of biologic processes.

 

Curr Diab Rep. 2008 Oct;8(5):393-8.Links
    Diabetes and the vitamin d connection.
    Holick MF.

    Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Boston University School of Medicine, 715 Albany Street, M-1013, Boston, MA 02118, USA. mfholick@bu.edu

    Vitamin D deficiency, which is common in children and adults, causes rickets, osteomalacia, and osteoporosis. Most organs and immune cells have a vitamin D receptor, and some also have the capacity to metabolize 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. 1,25-Dihydroxyvitamin D is a potent immunomodulator that also enhances the production and secretion of several hormones, including insulin. Vitamin D deficiency has been associated with increased risk of type 1 diabetes. Glycemic control and insulin resistance are improved when vitamin D deficiency is corrected and calcium supplementation is adequate. 25-Hydroxyvitamin D (measure of vitamin D status) of less than 20 ng/mL is vitamin D deficiency and 21 to 29 ng/mL is insufficiency. Children and adults need at least 1000 IU of vitamin D per day to prevent deficiency when there is inadequate sun exposure.

 

Oliver Gillie's reports on Vitamin D's benefits available online

Red

 

Reports describing Vitamin D3's benefits by Oliver Gillie,  a freelance medical researcher and writer, are available online.  

Here's the latest.  Note the recommendations by Drs Vieth, Holick, Holis, etc on pages III and IV.   It's a very interesting article, and one well worth the 30 minutes it takes to skim:

Scotland's Health Deficit:   An explanation and a plan

 

His older books can be viewed from here:

The Health Research Forum:  Reports

 

About the Author:

Oliver Gillie is a freelance medical researcher and writer. Formerly he was medical correspondent of The Sunday Times, then medical editor and later special correspondent of The Independent newspaper. He has a BSc and PhD degrees from Edinburgh University where he studied genetics and developmental biology under Professor C.H. Waddington at the Institute of Animal Genetics, Edinburgh. He also undertook research at the National Institute for Medical Research, Mill Hill, under Sir Peter Medawar. 

Red

By the way, although I believe the above reports make an important case for the involvement of low levels of Vitamin D3 in the pathogenesis of Multiple Sclerosis and other "autoimmune" diseases, IMHO, the expert researchers on Vitamin D3 may also be missing much of the reason for this, namely the importance of Vitamin D3 in controlling or preventing the infections that have been linked with these diseases.  

The article above mentions the antimicrobial peptides (cathelicidins) that so require Vit D3 for their production, but it really only mentions these cathelicidins in reference to tuberculosis.   The article also mentions Vit D3's importance for normal cellular apoptosis, but again it only mentions this in reference to cancer.  

IMHO, these researchers may be missing the importance of these two (and probably other) effects of Vit D3 in in controlling infections that may cause disease.   As we are aware, Vit D3 may influence levels of Chlamydia pneumoniae infection through its effects on the ability of the Chlamydia pneumoniae to prevent apotosis (and replicate protected inside a cell) for instance.   And cathelicidins may be important in keeping the henchmen Herpes viruses dormant, where they belong.

These researchers also don't seem to ever mention the relatively recently discovered importance of Leukotriene B4 for the induction of cathelicidins upon immune system detection of pathogens. What effects did the introduction of modern medicines that block the production of Leukotriene B4 so well and therefore significantly reduce the induction of already reduced levels of cathelicidins (due to low levels of Vit D3) upon immune system detection of pathogens have on disease rates?    I wonder...

Although I have no medical background, I personally believe the pathogenesis of many of the "autoimmune" diseases that these researchers point to heavy involvement of low levels of Vit D3 in their pathogenesis may actually be far more complex than these researchers realize.    Still, bless these researchers for the efforts!

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Red- thanks for your quick summary of the Vitamin D web here in terms of Cpn. Because of your interest in Leucotrines related to rosacea, you probably have a better grasp on this than any of us of these interactions.

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Sunlight, UV-radiation, vitamin D and skin cancer: how much sunlight do we need?

Sunlight, UV-radiation, vitamin D and skin cancer: how much sunlight do we need?
Adv Exp Med Biol. 2008;624:1-15.Links
   Sunlight, UV-radiation, vitamin D and skin cancer: how much sunlight do we need?
   Holick MF.

    Department of Medicine, Section of Endocrinology, Nutrition and Diabetes, Vitamin D, Skin and Bone Research Laboratory, Boston University Medical Center, 715 Albany Street, M-1 013, Boston, MA 02118, USA. mfholick@bu.edu

    Vtamin D is the sunshine vitamin for good reason. During exposure to sunlight, the utraviolet B photons enter the skin and photolyze 7-dehydrocholesterol to previtamin D3 which in turn is isomerized by the body's temperature to vitamin D3. Most humans have depended on sun for their vitamin D requirement. Skin pigment, sunscreen use, aging, time of day, season and latitude dramatically affect previtamin D3 synthesis. Vitamin D deficiency was thought to have been conquered, but it is now recognized that more than 50% of the world's population is at risk for vitamin D deficiency. This deficiency is in part due to the inadequate fortification of foods with vitamin D and the misconception that a healthy diet contains an adequate amount of vitamin D. Vitamin D deficiency causes growth retardation and rickets in children and will precipitate and exacerbate osteopenia, osteoporosis and increase risk of fracture in adults. The vitamin D deficiency has been associated pandemic with other serious consequences including increased risk of common cancers, autoimmune diseases, infectious diseases and cardiovascular disease. There needs to be a renewed appreciation of the beneficial effect of moderate sunlight for providing all humans with their vitamin D requirement for health.
Jim K Mon, 2008-04-07 22:52

The tolerability and biochemical effects of high-dose bolus vitamin D2 and D3 supplementation in patients with vitamin D insuffi

The tolerability and biochemical effects of high-dose bolus vitamin D2 and D3 supplementation in patients with vitamin D insufficiency.

Leventis P, Kiely PD.

Department of Rheumatology, St George's Healthcare NHS Trust, London, UK.

Objectives: To investigate the practicality and tolerability of high-dose intramuscular (i.m.) vitamin D2 or oral vitamin D3 replacement in vitamin D-insufficient patients, and to evaluate the biochemical efficacy of each formulation.

Methods: Sixty-nine patients with vitamin D insufficiency [25-hydroxyvitamin D (25(OH)D) <40 nmol/L] were recruited from the Rheumatology Outpatient Department of St George's Hospital, London.

In study 1, 50 patients received 300 000 IU i.m. vitamin D2 (ergocalciferol).

In study 2, 19 patients received 300 000 IU oral vitamin D3 (cholecalciferol) under observation.

Biochemical response was measured at baseline, and at 12 and 24 weeks. Results: Bolus i.m. vitamin D2 or oral vitamin D3 was well tolerated.

The change from baseline in serum 25(OH)D was significantly greater at 6 and 12 weeks in study 2 (p<0.0001 and <0.0001, respectively).

In study 1, a modest increase in mean serum 25(OH)D at 6, 12, and 24 weeks was observed but no patients achieved a serum 25(OH)D concentration >/=50 nmol/L. PTH remained elevated in 42% of patients with secondary hyperparathyroidism at 12 weeks.

In study 2, 100% and 89% of patients had serum 25(OH)D>50 nmol/L at 6 and 12 weeks, respectively.

All patients with elevated baseline PTH were fully suppressed at 12 weeks. No cases of hypercalcaemia were observed in either group.

 Conclusion: The 300 000-IU bolus of vitamin D2 or D3 was practical, well tolerated, and safe.

Vitamin D3 had greater potency than equimolar vitamin D2, with a higher, sustained serum 25(OH)D response and efficacious PTH suppression.

To adequately treat vitamin D insufficiency we would recommend administering 300 000 IU oral vitamin D3 approximately three times per year.

Daisy,  Thanks for this---it addresses a concern I've had as to whether or not taking D3 would exacerbate my already elevated calcium level.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Red

Good one, Daisy.  Thanks!

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Vitamin D Council and brief quote on Vit D in sarcoidosis

Vitamin D Council and brief quote on Vit D in sarcoidosis

The Vitamin D Council is an excellent source of information on Vitamin D, health and science (thanks Reenie:).

http://vitamindcouncil.org

Their research page is a useful listing of all the conditions in which insufficient Vitamin D has been linked to, including cancer, MS and autism. http://vitamindcouncil.org/research.shtml

Of interest to sarcoidosis patients looking to cautiously increase Vitamin D as part of a CAP for Cpn:

Hypersensitivity, Not Toxicity

Vitamin Di hypersensitivity syndromes are often mistaken for vitamin D toxicity. The most common is primary hyperparathyroidism. Other syndromes occur when abnormal tissue subverts the kidney's normal regulation of endocrine calcitriol production. Aberrant tissues, usually granulomatous, convert 25(OH)D into calcitriol causing high blood calcium. The most common such condition is sarcoidosis, oat cell carcinoma of the lung and non‑Hodgkin's lymphoma but other illness can cause the syndrome and they can occur while the patient's 25(OH)D levels are normal or even low. For that reason, while rare, it is advisable to seek a knowledgeable physician's care when repleting your vitamin D system, especially if you are older, have sarcoidosis, cancer or other granulomatous diseasesi. In such high‑risk patients, periodic monitoring of 25(OH)D levels and serum calcium will alert the physician to the need to do more tests, such as calcitriol or PTH, and take further action.

However, it seems clear that restoring physiological serum levels of 25(OH)D will help many more patients that it will hurt. In fact, living in America today while worrying about vitamin D toxicity is like dying of thirst in the desert while worrying about drowning.

http://www.vitamindcouncil.org/vitaminDToxicity.shtml

 

Jim K Thu, 2008-07-10 22:44

Vitamin D Inhibits Entry of Intracellular Pathogen

Vitamin D Inhibits Entry of Intracellular Pathogen

Although this is with a different intracellular pathogen than Cpn, it suggests one of the possible protective mechanisms that Vitamin D gives against intracellular pathogens. Like Cpn,  Mycobacterium tuberculosis infects the immune cells (macrophages) themselves, and this study describes the inhibition of cell invasion by Vitamin D.

J Microbiol Immunol Infect. 2008 Feb;41(1):17-25.

Synergistic action of vitamin D and retinoic acid restricts invasion of macrophages by pathogenic mycobacteria. Anand PK, Kaul D, Sharma M. Molecular Biology Unit, Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, India. BACKGROUND AND PURPOSE: Phagosomal maturation arrest is known to play a central role in the survival of pathogenic mycobacteria within macrophages. The maturation arrest of mycobacterial phagosome results from the retention of tryptophan-aspartate-containing coat protein (TACO) on this organelle, enabling successful replication of the pathogen. We have shown earlier that vitamin D(3) and retinoic acid (RA) down-regulate TACO gene transcription in a dose-dependent manner. METHODS: In this study, we analyzed the promoter region of TACO gene using bioinformatics tools and observed that the vitamin D receptor (VDR)/retinoid-X-receptor (RXR) response sequence was highly functional. We also evaluated the effect of treatment with vitamin D(3)/RA on Mycobacterium tuberculosis entry and survival in cultured human macrophages. RESULTS: TACO gene down-regulation observed with vitamin D(3)/RA treatment occurred through modulation of this gene via the VDR/RXR response sequence present in the promoter region of TACO gene. Treatment of macrophages with vitamin D(3)/RA allows maturation of mycobacterial phagosome, leading to degradation of the pathogen. CONCLUSIONS: Our results elucidate the mechanism of TACO gene down-regulation observed with vitamin D(3)/RA. Furthermore, the results revealed that vitamin D(3)/RA treatment inhibits mycobacterial entry as well as survival within macrophages, possibly through rescue of phagosome maturation arrest. The developing knowledge in this area suggests that vitamin D(3)/RA may be of importance in the treatment of intracellular infection, particularly tuberculosis.

Jim K Mon, 2008-09-08 15:48

Vitamin D Pathways - Importance of IL-15

Red

Here's another interesting area to keep an eye on, namely the apparent importance of IL-15 for bioconversion of 5-hydroxyvitamin D3 (25D3) into bioactive 1,25D3 and the downstream induction of cathelicidins:

"In this study, we found that TLR2/1-induced IL-15 was required for induction of CYP27b1, the VDR and the downstream antimicrobial peptide cathelicidin.  Although both IL-15 and IL-4 triggered macrophage differentiation, only IL-15 was sufficient by itself to induce CYP27b1 and subsequent bioconversion of 25-hydroxyvitamin D3 (25D3) into bioactive 1,25D3, leading to VDR activation and induction of cathelicidin"

Here's another study along these lines:

"Together, these results demonstrate that IL-15 plays an important role in antigen-induced neutrophil migration during inflammation, triggering a sequential OVA, IL-15, IL-18, MIP-2, MIP-1alpha, TNF-alpha, LTB4 and neutrophil migration signaling cascade"

 

There are quite a few other studies in pubmed showing the importance of IL-15 in fighting infections.  Here are a couple:

Unfortunately, some drugs seem to inhibit IL-15, and researchers are on the hunt for additional IL-15 inhibitors to treat "inflammatory" diseases:

 

 

 

 

 

 

 

 

Vitamin D Status: Measurement, Interpretation, and Clinical Application.

Vitamin D Status: Measurement, Interpretation, and Clinical Application.
 Ann Epidemiol. 2008 Mar 8 [Epub ahead of print]Click here to read Links
   Vitamin D Status: Measurement, Interpretation, and Clinical Application.
   Holick MF.

    From the Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Vitamin D, Skin and Bone Research Laboratory, Boston University Medical Center, Boston, MA.

    Vitamin D, the sunshine vitamin, is now recognized not only for its importance in promoting bone health in children and adults but also for other health benefits, including reducing the risk of chronic diseases such as autoimmune diseases, common cancer, and cardiovascular disease. Vitamin D made in the skin or ingested in the diet is biologically inert and requires 2 successive hydroxylations first in the liver on carbon 25 to form 25-hydroxyvitamin D [25(OH)D], and then in the kidney for a hydroxylation on carbon 1 to form the biologically active form of vitamin D, 1,25-dihydroxyvitamin D [1,25(OH)(2)D]. With the identification of 25(OH)D and 1,25(OH)(2)D, methods were developed to measure these metabolites in the circulation. Serum 25(OH)D is the barometer for vitamin D status. Serum 1,25(OH)(2)D provides no information about vitamin D status and is often normal or even increased as the result of secondary hyperparathyroidism associated with vitamin D deficiency. Most experts agree that 25(OH)D of < 20 ng/mL is considered to be vitamin D deficiency, whereas a 25(OH)D of 21-29 ng/mL is considered to be insufficient. The goal should be to maintain both children and adults at a level > 30 ng/mL to take full advantage of all the health benefits that vitamin D provides.
Jim K Mon, 2008-04-07 22:48

Vitamin D and skin physiology: a D-lightful story.

Vitamin D and skin physiology: a D-lightful story.
J Bone Miner Res. 2007 Dec;22 Suppl 2:V28-33.Click here to read Links
   Vitamin D and skin physiology: a D-lightful story.
   Holick MF, Chen TC, Lu Z, Sauter E.

    Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Vitamin D, Skin, and Bone Research Laboratory, Boston University Medical Center, Boston, Massachusetts, USA.

    Throughout evolution, exposure to sunlight and the photosynthesis of vitamin D(3) in the skin has been critically important for the evolution of land vertebrates. During exposure to sunlight, the solar UVB photons with energies 290-315 nm are absorbed by 7-dehydrocholesterol in the skin and converted to previtamin D(3). Previtamin D(3) undergoes a rapid transformation within the plasma membrane to vitamin D(3). Excessive exposure to sunlight will not result in vitamin D intoxication because both previtamin D(3) and vitamin D(3) are photolyzed to several noncalcemic photoproducts. During the winter at latitudes above approximately 35 degrees , there is minimal, if any, previtamin D(3) production in the skin. Altitude also has a significant effect on vitamin D(3) production. At 27 degrees N in November, very little ( approximately 0.5%) previtamin D(3) synthesis was detected in Agra (169 m) and Katmandu (1400 m). There was an approximately 2- and 4-fold increase in previtamin D(3) production at approximately 3400 m and at Everest base camp (5300 m), respectively. Increased skin pigmentation, application of a sunscreen, aging, and clothing have a dramatic effect on previtamin D(3) production in the skin. It is estimated that exposure in a bathing suit to 1 minimal erythemal dose (MED) is equivalent to ingesting between 10,000 and 25,000 IU of vitamin D(2). The importance of sunlight for providing most humans with their vitamin D requirement is well documented by the seasonal variation in circulating levels of 25-hydroxyvitamin D [25(OH)D]. Vitamin D deficiency [i.e., 25(OH)D < 20 ng/ml] is common in both children and adults worldwide. Exposure to lamps that produce UVB radiation is an excellent source for producing vitamin D(3) in the skin and is especially efficacious in patients with fat malabsorption syndromes. The major cause of vitamin D deficiency globally is an underappreciation of sunlight's role in providing humans with their vitamin D(3) requirement. Very few foods naturally contain vitamin D, and those that do have a very variable vitamin D content. Recently it was observed that wild caught salmon had between 75% and 90% more vitamin D(3) compared with farmed salmon. The associations regarding increased risk of common deadly cancers, autoimmune diseases, infectious diseases, and cardiovascular disease with living at higher latitudes and being prone to vitamin D deficiency should alert all health care professionals about the importance of vitamin D for overall health and well being.
Jim K Mon, 2008-04-07 22:50

Vitamin D and the immune system: role in protection against bacterial infection.

Curr Opin Nephrol Hypertens. 2008 Jul;17(4):348-52.

Veterans Affairs Medical Center, San Francisco, California 94121, USA. Daniel.bikle@ucsf.edu

PURPOSE OF REVIEW: The role of vitamin D extends well beyond that of regulating calcium homeostasis. One of these areas is immune function. Immunity is both adaptive and innate, and vitamin D signaling is operative in both. This review will examine these actions of vitamin D, in particular the role of vitamin D in host defense against infection. RECENT FINDINGS: This review will consider two examples of vitamin D-regulated innate immunity that have been recently explored: the role of vitamin D signaling within macrophages to enable them to respond to and kill Mycobacterium tuberculosis organisms, and the role of vitamin D signaling in the keratinocytes of the epidermis to enable them to respond to disruption of their barrier function. Potential application to periodontal disease will then be considered. SUMMARY: Both adaptive and innate immune processes are two edged: beneficial and harmful. Although suppression of adaptive immunity may be beneficial in a number of self-destructive diseases, such suppression may predispose to infection. Enhancement of innate immunity is clearly beneficial in diseases like tuberculosis, but potentiation of proinflammatory processes can increase tissue destruction as in bone loss in periodontal disease. The balance, however, favors adequate vitamin D nutrition in host defense against infection.

Wonderful Paper on Vitamin D, with focus on Vitamin D and the Nervous System

Red

 

This is a wonderful Academic Dissertation by Anna Minasyan, from Tampere University Medical School:

Vitamin D and the Nervous System

It contains an amazingly complete and fairly easy to read (if you can skim through all the citations) review of the known actions of Vitamin D in the body, including very good explanations of the known pathways.   Here are a few sections that I believe are particularly important:

  • Section 5.1.3 Vitamin D receptors - this section gives a very clear explanation of how Vit D metabolites enter cells and bind to Vitamin D receptors (VDRs) in the cell nucleus to influence cell function.   As I've said before, I believe this is likely the mechanism that provides the greatest effect of Vit D over Cpn infection.   That is, I believe strongly that it is likely through this mechanism that Vit D short circuits intracellular forms of Cpn's influence over cellular apoptosis mechanisms (via NF-KappaB and inhibitor of apoptosis proteins), making it much more difficiult for Cpn to "hijack" cells and replicate safely inside them.   See here for more.
  • Section 5.2 Effects of Vitamin D on the Nervous System - this section, I believe, is a must read for those with CNS issues related to Cpn.  Some points of interest:
    • Vit D "participates in modulation of CNS detoxification pathways through regulation of y-Glutamyl transpeptidase, an enzyme which up-regulates the glutathione pool and reduces the production of reactive nitrogen species in astrocytes"
    • Vit D "may inhibit the synthesis of inducible nitric oxide synthase (iNOS), an enzyme which is produces in response to inflammatory stimuli and have harmful effexts on the CNS"
    • Vit D "may protect the structure and integrity of neurons through neurotrophin (NT) synthesis and nerve growth factor (NGF)"
  •  Section 9.4 The Role of VDR in Hearing (III) - while probably more interesting than important, this section is interesting in that Vit D's importance for preventing and possibly correcting hearing loss in not as widely publicized as other known functions of Vit D.